This project will examine the neural bases of emotion regulation and dysregulation in samples of adolescents selected on the basis of their risk status for internalizing disorder. Adolescent is a period during which risk for anxiety and mood disorders increases substantially and little is known about the brain mechanisms responsible for vulnerability to these disorders. We will take advantage of extensive data collected within two longitudinal cohorts that will be a central feature of this Center. From these cohorts, three samples will be tested. One sample consists of 85 individuals from Project 2 who underwent fMRI scanning using virtually the identical tasks when they were 14 years of age. A second sample, also derived from Project 2 (Essex), will include participants who will be selected to vary in levels of basal cortisol early in life (age 4.5 years) and later in early adolescence. In another cohort derived from Project 3 (Goldsmith) monozygotic and dizygotic twin pairs will be selected in which one member of the pair has high levels of internalizing symptoms. Both concordant and discordant pairs will be selected in this manner. All participants will undergo a scanning session during which functional MRI will be obtained while participants engage in two tasks. One task will assess the neural correlates of both voluntary and automatic emotion regulation while the other task will be a face go-no-go task that assesses sensitivity to different facial expressions of emotion and inhibitory control in the face of emotional distracters. During scanning, electrodermal and pupillary measures will be obtained, in addition to eye tracking. In addition, participants will be administered an automated version of a task designed to assess working memory capacity (O-span) to ascertain the relation between individual differences in working memory capacity and emotion regulation. We will test the hypothesis that adolescents selected to be vulnerability to internalizing disorders (either because of cortisol profiles or symptoms of anxiety) will exhibit evidence of the poor emotion regulation expressed as high levels of amygdala activation and low levels of activation in ventromedial prefrontal cortex during instructions to down-regulate negative affect. A similar pattern is expected during the task phase designed to assess automatic emotion regulation. The face go-no-go task will allow us to test the hypothesis that adolescents at increased risk for internalizing disorders will show increased sensitivity to fear and angry faces and show a more conservative response bias (inhibiting their response to faces other than the target); moreover these individuals are predicted to show increased activation in the right inferior frontal gyrus, a region in which we have previously found to correlated with social anxiety. The findings from this project will provide novel new evidence on the neural bases of emotion regulation and dysregulation in adolescence and will showcase the role of these processes in vulnerability to anxiety and mood disorders.